As is well known, the human heart has four chambers for receiving blood and for pumping it to various parts of the body. In particular, the two upper chambers of the heart are called atriums, and the two lower chambers are called ventricles.
During normal operation of the heart, oxygen-poor blood returning from the body enters the upper right chamber known as the right atrium through the superior vena cava and inferior vena cava. The right atrium fills with blood and eventually contracts to expel the blood through the tricuspid valve to the lower right chamber known as the right ventricle. Contraction of the right ventricle ejects the blood in a pulse-like manner from the right ventricle to the pulmonary artery which divides into two branches, one going to each lung. As the oxygen-poor blood travels through the lungs, it becomes oxygenated (i.e. oxygen-rich).
The oxygenated blood leaves the lungs through the pulmonary veins and fills the upper left chamber of the heart known as the left atrium. When the left atrium contracts, it sends the blood through the mitral valve to the lower left chamber called the left ventricle. Contraction of the left ventricle, which is the stronger of the two lower chambers, forces blood through the main artery of the vascular system known as the aorta. The aorta branches into many smaller arteries and blood vessels that eventually deliver the oxygen-rich blood to the rest of the body.
As is apparent from the description above, the proper sequence of contraction and relaxation of the heart chambers is fundamental to its operation. Contraction of the heart chambers is controlled by the heart's conduction system, which includes areas of specialized "nodal" tissue or "nodes" capable of generating and transmitting electrical impulses. The ability to generate electrical impulses is known as "automaticity."
The natural pacemaker of the heart is called the SA (sino-atrial) node. It lies in the groove where the superior vena cava joins the right atrium. The SA node contains two types of cells, one of which exhibits automaticity.
In general, the conduction of an electrical impulse generated by the SA node proceeds as follows. The cardiac impulse travels across the walls of the atria, eventually causing the atria to contract. The impulses generated by the SA node are also transmitted to the atrio-ventricular (AV) node located in the lower portion of the right atrium near the right ventricle. From the AV node, the impulses travel through another area of nodal tissue known as the bundle of His and eventually to the Purkinje's fibers that envelop the ventricles. When the impulses reach these fibers, they cause the ventricles to contract.
More specifically, from the SA node the cardiac impulse spreads radially along ordinary atrial myocardial fibers. A special pathway, the anterior interatrial myocardial band, conducts the impulse from the SA node directly to the left atrium. In addition, three tracts, the anterior, middle, and posterior internodal tracts or pathways constitute the principal routes for conduction of the cardiac impulse from the SA to the AV node. These tracts consist of ordinary myocardial cells and specialized conducting fibers.
The AV node is situated posteriorly on the right side of the muscle wall dividing the heart's right and left atria, (known as the interatrial septum). The AV node also contains cells that exhibit automaticity. The AV node receives and relays the impulses through the septum to a cluster of fibers between the ventricles known as the bundle of His.
The bundle of His passes down the right side of the inter ventricular septum (the muscle wall between the right and left ventricles) and then divides into the right and left bundle branches. The right bundle branch is a direct continuation of the bundle of His and it proceeds down the right side of the interventricular septum. The left bundle branch, which is considerably thicker than the right, branches almost perpendicularly from the bundle of His and bisects the interventricular septum. On the surface of the left side of the interventricular septum the main left bundle branch splits into a thin anterior division and a thick posterior division.
The right bundle branch and the two divisions of the left bundle branch ultimately subdivide into a complex network of conducting fibers called Purkinje's fibers which envelop the ventricles.
As an impulse travels from the region of the atria to the ventricles, the first portions of the ventricles to be excited are the interventricular septum and the papillary muscles. The wave of activation spreads to the septum from both its left and its right endocardial surfaces (the inner membrane of the heart wall). Early contraction of the septum tends to make it more rigid and allows it to serve as an anchor point for the contraction of the remaining ventricular myocardium (the middle layer of muscle that comprises the heart wall).
The endocardial surfaces of both ventricles are activated rapidly, but the wave of excitation spreads from endocardium to the outer membrane or sheath of the heart wall known as the epicardium at a slower velocity. Because the right ventricular wall is appreciably thinner than the left, the epicardial surface of the right ventricle is activated earlier than that of the left ventricle. The last portions of the ventricles to be excited are the posterior basal epicardial regions and a small zone in the basal portion of the interventricular septum.
Cardiac arrhythmia refers to a disturbance in the rhythm of contraction and relaxation of the heart's chambers. In cardiac arrhythmia, the atria and/or ventricles do not contract and relax in the regular and sequential pattern described above, and may instead contract prematurely and/or randomly. In the most serious types of arrhythmia, such as fibrillation, the impulses may fragment into multiple, irregular circuits which are incapable of causing coordinated contractions of the heart chamber and, therefore, may adversely affect the pumping of blood.
Various causes of arrhythmia have been identified. One cause of cardiac arrhythmia may be a disorder in the formation of the impulse. For example, although the primary source of impulse formation is the SA node, it is known that most cardiac cells are capable of exhibiting automaticity. If an impulse traveling, for example, from the SA node is delayed or diverted, other cardiac cells or clusters of cells outside the areas of nodal tissue may spontaneously initiate an impulse. These cells or cell clusters are known as ectopic foci. The impulses generated by ectopic foci may be transmitted to the atria and/or ventricles prior to the impulse that is traveling along the normal conductive pathway, thereby causing premature contraction of the heart chamber.
Arrhythmia may also be caused by disorders in the conduction or transmission of an impulse from one region of the heart to another region. In this case, injury to a section of the heart tissue that is part of the normal conductive pathway may slow, block or even divert transmission of the impulse from its normal path. Impulses traveling along a different pathway proximal to the blocked pathway may attempt to reenter the blocked pathway. If the impulse reenters the blocked pathway, it may prematurely stimulate other nodal tissue causing the atria or ventricles to contract before these chambers have returned to their relaxed state.
One known method of treating cardiac arrhythmia, includes ablating the focal point of the arrhythmia within the heart tissue with the tip of a catheter or other surgical device. The devices used for treating arrhythmia typically have elongated, small diameter tubular bodies that include tips that can be heated, super-cooled or are capable of emitting radiofrequency energy. Typically, the device is introduced and advanced through the vascular system of the patient until the tip of the device reaches the desired location (e.g. the suspected source of the arrhythmia for treatment). When applied to the source of the arrhythmia, these heated, super-cooled or otherwise energized catheter tips ablate the section of tissue responsible for the cardiac arrhythmia.
One such method for treating disorders associated with the conduction of electrical signals in cardiac tissue is described in U.S. Pat. No. 4,641,649. There, an antenna located at the distal tip of the catheter receives electrical signals from the heart which aids the physician in determining the source of the cardiac disorder. Once the source has been located, radiofrequency or microwave frequency energy is applied to the section of tissue through the tip of the catheter to ablate the source of the electrical disorder. The ablation can be controlled by means of an attenuator which regulates the amount of power radiated by the antenna.
Another example of a method and apparatus for ablating a portion of body tissue is described in U.S. Pat. No. 5,147,355. There, a catheter is guided through the patient's body to the area of tissue to be ablated. An electrode located at the catheter tip monitors electrical activity of the tissue and transmits the information to a monitor display. After the physician has positioned the tip of the catheter at the suspected source of the arrhythmia, the tip of the catheter is cryogenically super-cooled to ablate the desired section of heart tissue. The device in this patent includes a flow control valve to regulate the amount of cryogenic liquid delivered to the catheter tip, and thereby try to control the temperature and rate of tip cooling. It is unclear from the description in U.S. Pat. No. 5,147,355 how or whether the operator is able to determine the tip temperature. If during the course of cryoablation, an arrhythmic signal continues to be detected by the electrode, the cryoablation may be curtailed and the catheter tip repositioned to cryoablate another section of tissue suspected of being the source of the arrhythmia.
The catheter described in U.S. Pat. No. 5,147,355 includes first and second concentric fluid flow passages adjacent the tip portion for the flow of cryogenic fluid. Accordingly, the flow passages of the catheter must be made of a rigid material such as stainless steel or other material capable of withstanding the high pressures and temperatures as low as -60.degree. C. associated with liquid-to-gas phase change in a cryogenic fluid. As a result, the catheter is necessarily less flexible and more difficult to maneuver than is desirable when advancing the catheter through the vascular system of a patient.
One of the drawbacks with the above-described method for treating cardiac arrhythmia is that it does not allow for precise control of the probe tip temperature. For example, in the cryoablation method described in U.S. Pat. No. 5,147,355, the temperature of the catheter tip is regulated by the amount of cryogenic fluid delivered to the catheter tip. Using this method, change in the temperature of the probe tip is gradual, and rapid and precise temperature adjustment to the probe tip over a broad range of temperatures is difficult to achieve. The inability to quickly adjust the probe tip temperature may result in some destruction of sections of heart tissue that are not responsible for the arrhythmia.
Although it is known that cooling the heart tissue can cause observable changes in the electrical activity of the heart, Hariman et al., "Cryothermal Mapping of the Sinus Node in Dogs: A Simple Method of Localizing Dominant and Latent Pacemakers," Cardiovascular Research, 1989, Vol. 23, pp. 231-238 and Gessman, "Localization and Mechanism of Ventricular Tachycardia by Ice-Mapping 1-Week After the Onset of Myocardial Infarction in Dogs," Circulation, Vol. 68, No. 3, September 1983, pp. 657-666, which are incorporated by reference herein, the present methods for treating arrhythmia, as described above, typically have not utilized cooling of the heart tissue for purposes of identifying the foci of the aberrant signals, but have used low-temperature cooling for ablation.